1. Field of the Invention
The present invention relates to a feed composition for breeding pigs in order to produce pork rich in n-3 fatty acid and more particularly, to a feed containing about 70 to 90% by weight of an n-3 fatty acid source, about 10 to 20% by weight of carbohydrate source, about 0.1 to 1.0% by weight of an agent for promoting a decrease in the cholesterol level, and about 0.1 to 1.0% by weight of an antioxidant, which is rich in n-3 fatty acid which is beneficial to humans and further can prevent various physiological disorders caused by pork having a high n-6 fatty acid content.
2. Description of the Prior Art
In pork presently on the market, the content of n-3 fatty acid is around 1% and the content of n-6 fatty acid is approximately 15 to 30%. Unfortunately, n-6 fatty acid may act as to cause various adverse physiological effects. For this reason, the field of Chinese medicine has warned against the bad effects of pork and the general public has often been warned to avoid the intentional intake of pork.
As shown in Table 1 below, 18:2.sub.n-6 as n-6 fatty acid is metabolized to arachidonic acid which is then further metabolized in the cell membranes of body tissues. It has been recognized that various metabolites produced due to the excessive intake of n-6 fatty acids, i.e., eicosanoids such as 2-series prostaglandins and 4-series leukotrienes, may cause various physiological disorders such as atherosclerosis, hypertension, myocardial infarction, ischemia, thrombosis, heart disease, osteomyelitis and skin disease.
However, 18:3.sub.n-3 as n-3 fatty acid is converted into eicosapentaenoic acid (EPA) in the cell membrane of body tissue and then EPA produces 3-series prostaglandins and 5-series leukotrienes through metabolism.
The 3-series prostaglandins and 5-series leukotrienes thus produced block the production of 2-series prostaglandins and 4-series leukotrienes produced by the metabolism of arachidonic acid, and thus prevent various physiological disorders caused by excessive 2-series prostaglandins and 4-series leukotrienes. Further, n-3 fatty acid itself blocks the metabolic pathway of n-6 fatty acid, as shown in Table 2 below, and therefore, inhibits the production of eicosanoids from n-6 fatty acid.
TABLE 1 __________________________________________________________________________ Metabolic pathway of arachidonic acid ##STR1## ##STR2## ##STR3## ##STR4## __________________________________________________________________________
TABLE 2 ______________________________________ Inhibition of n-6 fatty acid metabolic pathway by n-3 fatty acid ##STR5## ______________________________________
In Biochimica et Biophysica Acta (1989) 1001:25-30, the present inventors have reported that when EPA as n-3 fatty acid is administered to a Sprague-Dawley rat, the amount of arachidonic acid, as n-6 fatty acid, present in cell membranes, is reduced drastically.
In another reference, Biochimica et Biophysica Acta (1989) 1006:9-11, the present inventors reported, as the result of investigation on the biosynthesis of various fatty acids in experimental animals to which EPA is administered and then (.sup.3 H) glycerol is injected, that the synthesis of arachidonic acid as n-6 fatty acid is drastically reduced whereas the content of EPA and DHA (docosahexaenoic acid) as n-3) fatty acid increases significantly.
Furthermore, the present inventors disclose in Lipids (1990) 25:811-814, that after EPA administration, the biosynthesis of liver fat in Sprague-Dawley rats decreased by about 40 percent.